Certain plasmids (i.e., non-chromosomal genetic elements of bacteria) affect bacterial mutation in various ways; some plasmids increase the frequency of some classes of spontaneous mutation. Some such plasmids also increase the number of mutations induced by a given exposure to ultraviolet irradiation, or to chemical mutagens and reduce the killing effect of such exposure. Plasmids do not produce these effects in host deficient of recA function, but are not dependent on some other bacterial genes involved in repair of damaged DNA. It is surmised that plasmids which enhance the mutagenic effect of physical and chemical treatments do so by increasing the activity of a bacterial system for repair of chemically altered DNA which is "error-prone." Most chemicals known to produce cancer in man or animals produce mutations in appropriate bacteria, and most chemicals mutagenic for bacteria which have been adequately tested have proved to be carcinogenic. The Ames system comprises a set of auxotrophic bacterial strains by genetic manipulation made highly responsive to the mutagenic effect of many chemicals; some of the tester strains carry plasmid pKM101, which greatly enhances their mutational response to various chemicals. However, the system does not detect mutagenic activity in some known or suspected carcinogens. We propose to test other plasmids in various auxotrophic salmonella typhimurium strains, wild-type or with mutations affecting UV sensitivity, and to investigate the effect of each plasmid on spontaneous mutation frequency, and for enhancement of mutagenic effect of exposure to UV or visible light or to various chemicals known or suspected to be carcinogens and/or mutagens, with the object of: (1) discovering the mechanism by which plasmids affect mutation, spontaneous or induced; (2) finding plasmids which will enable tester strains to detect the expected, but so far not observed, mutagenic effect of certain carcinogens.